Nitric Oxide Modulates Ca²⁺ Leak and Arrhythmias via S-Nitrosylation of CaMKII.

ABSTRACT:

Background

Nitric oxide (NO) has been identified as a signaling molecule generated during β-adrenergic receptor stimulation in the heart. Furthermore, a role for NO in triggering spontaneous Ca²⁺ release via S-nitrosylation of CaMKIIδ (Ca²⁺/calmodulin kinase II delta) is emerging. NO donors are routinely used clinically for their cardioprotective effects on the heart, but it is unknown how NO donors modulate the proarrhythmic CaMKII to alter cardiac arrhythmia incidence. We test the role of S-nitrosylation of CaMKIIδ at the Cysteine-273 inhibitory site and cysteine-290 activating site in cardiac Ca²⁺ handling and arrhythmogenesis before and during β-adrenergic receptor stimulation.

Methods

We measured Ca²⁺-handling in

SUBMITTER: Power AS 

PROVIDER: S-EPMC10699507 | biostudies-literature | 2023 Dec

REPOSITORIES: biostudies-literature